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GI GU TEST ONE
A. Renal Functions
excretion of body metabolism end-products
urea
creatinine
uric acid
body fluid constituent concentration control (electrolyte and water balance)
blood volume maintenance
detoxification
endocrine regulation of ECV
control of REC mass
B. Influencing Hormones
Parathyroid hormone (PTH)(triggered by ca+ in serum)
enhances absorption of Ca & Mg in the PT
inhibits phosphate and bicarbonate absorption
stimulates renal conversion of 25- dihydroxycholecalciferol
Aldosterone stimulates NA+ absorption in the (DT)
increases net KA+ and H+ secretion in
the DT andcollecting tubule
ADH promotes formation of hypertonic urine incr.s H2O resorption in the
collecting duct
Erythropoetin stimulates RBC production in the marrow
secreted by the JG cells in response to a reduction in renal perfusion
Renin pressure (low tubuar chloride concentration)
stimulates the renin angiotensin mechanism (constriction of the efferent
arterioles)
)
C. The Nephron
the functional unit of the kidney
Glomerulus (leaky) AKA cap. tuft
through which fluid is filtered
located in the cortex of the kidney
filtration is dependent upon the hydrostatic pressure and the molecular size ( more blood faster
over hydration flow -> less absorption -> lower
serum BUN
Increased due to decreased renal renal failure '~
blood flow urinary obstruction
dehydration
hypotension
renal artery stenosis
pregnancy
Panic value >100 m/dl
C. Serum BUN Level Factors of tubular flow
Rate of flow Absorption Serum BUN
Fast Less Low
Slow More High
BUN/Creatinine Ratio
the liver doesn't affect creatinine
an increase or decrease in this ratio may be due to renal failure but may depend upon the type
of renal failure
Normal BUN l -20 mg/ dl
Normal serum creatinine 0.5 - 1/5 mg/ dl
Greater than 20:1 renal failure
cardiovascular failure
Less than 20:1 Renal failure
Azotemia - elevation of urea in the blood
B. Pathophysiology
volume depletion
acute tubular necrosis
hepatorenal syndrome
C. Types of Azotemia
Pre-renal
common
due to problem before the kidney that decreases flow to the kidneys
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possible causes
hypotension
steroids
embolus
flap of tissue
common lab values
BUN=80
Creatinine--OS
Renal
common
problem lies in the kidney (nephron)
nephritis may cause this
common lab values
BUN=40
creatinine = 2.0
Post-renal
problem lies after the kidney (e.g. blockage due to stenosis)
bladder outlet, prostatitis
history of blockage usually noted
chronic predisposition
A. Mechhanism
Cellular Involvement
macula densa cells
located in the lining of the inner portions of the diluting segment juxtaglomerular (JG) Cells
lining of the afferent & efferent arterioles
release renin
B. Initiation of Renin-Angiotensin System
macula densa cells detect low chloride concentration in the diluting segment
macula densa cells stimulate the JG cells
JG cells secrete renin
C. functions
in the collecting tubule and last 1/2 of distal tubule:
increases sodium reabsorption
increases potassium secretion
increases water reabsorption due to the effects of increased sodium resorption
A. Dip Stick Test
easiest method for urinalysis
a qualitative method of analysis (not quantitative)
a time dependent method
B. Analysis
Color and Appearance
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clear or amber normal
cloudy dehydration
infection
tea color or brown hemolysis
liver disease
biliruibin
bleeding
brown & cloudy RBC involvement (bleeding)
Specific Gravity
normal = 1~0O3-l.030
indication of urine concentration
high specific gravity
state of dehydration (e.g wrestlers)
low specific gravity
brain trauma
low ADH (dilute urine)
Urobilinogn
increased levels indicates problem with liver function
Blood
when present in urine, always considered an abnormal finding
Bilirubin
elevated level indications hemolysis
liver disease
C. Functions
in the collecting tubule and last 1/2 of distal tubule:
increases sodium reabsorption ~
increases potassium secretion ~
increases water reabsorption due to the effects of increased sodium resorption
Ketone
indication 0f lipolysis
common associated conditions
diabetes
high fat diets
starvation
Glucose
normal serum glucose = 80-120 mg/ dl U normal urine glucose = 0
100% absorbed in the proximal tubule
increased urine glucose levels indicates diabetes
result of exceeding the tubular load for glucose
glucose threshold = 300 mg/ dl blood glucose
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tubular load for glucose =300 mg/ min
Protein normal urine levels
less than 150 mg/ 24 hours
the tubular load for protein = 0
increased urine concentration indications
neplirotic syndrome (>3 -5 g / 24 hours)
carcinoma
nephron disease
post exercise (vigorous; normal)
starvation
pregnancy (normal)
Urine pH U normal =5.5-6.0
alkaline urine
indicates a gram negative infection
pseudomonas
proteus
Urine Sediments
A. Cellular Sediment
Red Blood Cells
normal =0-2/ HPF
lower urinary tract bleeding yields too many to count
UT bleeding sites
bladder, urethra
glomerulus
tubules
renal pelvis
White Blood Cells
normal =0-2/ HPF
infection increases WBC count
WBC's do not normally pass through the glomerulus
pyuria (>5-10 WBC/ HPF)
Epithelial Cells
increased levels indicate upper UT involvement
acute glomerular nephritis (glomerular destruction)
acute tubular necrosis (tubular destruction)
extensive dehydration
Bladder Cells
large oval squamous epithelial cells
increased levels with infection
Yeast
similar in size to the WBC with a spiculated appearance
usually indicative of a "bad catch" (not mid-stream)
commonly found at the end of the urethra
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Bacteria
bacteriuria (5 RBC) azotemia
Numerous WBC UTI
Granular casts associated with renal disease
Bacteria UTI (culture confirmation)
Crystals Significance
Cystine cystinuria diagnosis
Calcium phosphate alkaline urine
Calcium oxalate may appear in normal urine as it cools
Uric acid may appear in normal urine as it cools
Triple phosphate UTI
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NORMAL VALUES
Characteristics and Chemical Determination Micro exam of the sediment
Measurements
PH Glucose (-ve) casts (-ve)
4.6-6.8 (average =6) some hyaline
Ketones (-ve)
Turbidity RBC (rare)
o clear to slightly hazy Blood (-ve)
Crystals (-ve)
Specific Gravity Protein (-ve)
o 1.015-1.025 with normal fluid WBC's (-ve or rare)
intake Bilirubin (-ve)
Normal color = yellow Urobilinogen (0.1-1)*
amber color indicates
high specific gravity Nitrate for bacteria (-ve)
small urine output
Leukocyte esterase (-ve)
Renal Failure
Decrease in Glomerular filtration
sudden stopping of urine flow or
just not getting the good stuff
Stages of Renal Failure
prodromal
ologouric - less than 500 ml/day
post oligouric
Acute Renal failure (ARF)
bilateral process
sudden cessation of urine flow(occurs with in days)
rapid regression (weeks to a couple of mpnths)
good prognosis (90% recovery) - gradually recover (weeks to monts)
causes
scondary to drugs
secondary to glomerular or tubular damage
Types
Acute Glomerular nephritis (AGN)
Acute Tubular Necrosis
Clinical Signs
edema
weight gain
oligouriia
incr. BUN
anorexia
pulmonary edema
nausea & vomitting
hematuria
hyperreflexia
Pre-renal
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caused by anything that compromises the blood supply
Most common cause is hypovolemia
History
rapid weight loss
flu-like symptoms
lack of ingestion
bleeding
diuretic therapy
burns
Post Renal
bilateral ureteral obstruction
calculi
thrombus
neoplasm
Urethral obstruction (commonly unilateral)
prostatic hypertrophy
prostatitis
tumors of the bladder & prostate
calculi
Intra renal
glomerular inflammation
blood vessel involvement
vasculitis
malignant hypertension
eclapsia
History
multisystem disease
fever
HTN
hematuria
Acute Glomerular Nephritis (AGN)
A. Definition
0 an acute and diffuse inflammation of the glomerulus
0 involves almost all of the glomeruli with the exception of the tubules
0 a. k. a. Acute Nephrilic Syndrome
0 not an inflammation of the kidney itself
o it is a systemic reaction. An antigen reaction occurs that adheres to the basement membrane
B. Prevalence
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Sex
0 male > female (60:40)
A~
~, children affected more than adults represents 0.5% (1/ 200) of all hospital admissions more common than ATN
C. Etiology of AGN
o secondary to bacterial infection
o group A Beta Hemolytic Sfreptococcus represents the most common etiologic agent of AGN
o the infection usually is found somewhere else in the body
upper respiratory infections are the most common (e.g. strep throat)
the severity of the strep infection is not related to the severity of the kidney inflammation o site preference for
strep infections
kidney - yields AGN
myocardium - yields endocarditis
0 typically occurs 1-5 weeks before onset of ACIN
o wounds
o skin infections
O malaria
o viral infections (e.g. measles)
D. Pathophysiology of AGN
antigen antibody complexes are formed & block the glomerulus
the Ag/ Ab complex binds to the basement membrane of the glomerulus
yields swelling of the basement membrane, capillaries, & Bowman's capsule due to a hypersensitivity reaction
eosinophils WBC's migrate to area
WBC cast formation as a result of hypercellularity
a latent or dormant period of 1-4 weeks following a primary infection is required for the Ag / Ab complexes to form
E. Clinical Features of AGN
0 fatigue
0 malaise
0 flu-like symptoms
0 GI symptomotology
anorexia
vomiting
nausea
abdominal cramping
0 pain upon palpation over the kidney region
positive Murphy's punch test
fever
present during initial phase of infection (returns to normal)
low-grade (4 grams/ day = nephrotic syndrome
H. Treatment of AGN
anti-inflammatory substances
metabolic support
purpose is to decrease side effects and symptoms
most patients recover
Acute Tubular Necrosis
A. Definition
a disease affecting the tubules
the glomerulus is involved only with chronic conditions
B. Etiology
Renal Toxins
common agents
mercury
carbon tetrachloride (dry cleaning agent of yester-year)
ethylene glycol
drugs
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aminoglycosides (for tx of gram negative infections)
concentrated in the proximal tubules and cause diffuse tubular cell necrosis
the basement membrane is affected last & therefore the disease process is more recoverable than the
ischemic type of ATN
Exogenons renal toxins
toxin ingestion
skin absorption (. DMSO)
injected toxins
aminoglycosides
streptomycin
heavy metals
iodinated radio contrast agents
Endogenous renal toxins
Hemoglobin as a result of hemolysis
Hg collects in the tubules & binds to the basement membrane
Myoglobin from crushing injuries
myogiobin is released and precipitates in tubules
Ischemia
the most common cause of ATN
usually due to hypotension ~
lack of oxygen supply affects the capillaries & basement membrane before affecting the
tubular cells and therefore the recovery is guarded compared to the toxin type of ATN
the ischemia has a regional distribution (wedged shaped area of necrosis)
kidneys & nephrons have random involvement
nephron & cortical involvement is directly related to irreversibility
ischemic ATN has worse prognosis than renal toxin ATN because we cannot produce
collateral vessels fast enough
hypotension - most common cause
Shock
too low of a blood pressure to sustain
secondary to anything
e.g. gram negative bacteria
burns
physiological cycle
protein -> Low blood volume -> Low renal flow ->
interruption of blood flow to kidneys
hemorrhage
tumor
aortic dissecting aneurysm
infarct
pregnancy
drugs (e.g. diuretics)
blood clots
eclampsia
uterine compression of renal artery
catecholamine release Vasoconstriction of afferent arteriole
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drug / chemical effect
diuretic protocol -> excess fluid loss -> low BP -> vasoconstriction plus toxicity to basement membrane
blood clots
C. Clinical Features of Early Tubular Necrosis
Oliguria
3O - 4O ml / day
occurs during the first couple days
factors
plugging of the nephrons & tubules by casts; hydrostatic pressure builds up in Bowman's capsule,
therefore nothing is filtered in
inflammation of the tubules closes off the tubules
Fever
low grade fever for the first day or two
fever regresses when inflammation regresses
less than lOl0 F
Blood changes
increased WBC's at site of tissue injury
occurs due to inflammation of the tubules but disappears in the first week
increased serum amylase & lipase
DDx must include acute pancreatitis
increased BUN (urea)
due to decreased urine flow
rapid rise in BUN levels (as much as 50 mg/ 100 mil day)
normal level = 10-20 mg/ 100 ml
levels may approach 100-200 m~ 100 ml
occurs in the first couple of days
D. Clinical Features of Late ATN
Edema due to decreased fluid loss (oliguria)
check ark:les
Oliguria not as pronounced as the early stages of ATN
200-500 mi/day (normal = 1000-1500 mil day)
increased specific gravity
Nausea due to edema in the GI tract & systemic acidosis
Anorexia due to:
edema of the GI tract
azotemia (70-80 mg/ dl of urea)
acidosis
Lethargy & Weakness due to:
acidosis (uric acid affects membranes)
azotemia (increased BUN)
increased serum potassium levels
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Increased thirst due to renin angiotensin mechanism activation
from increase in osmotic gradient
Urine casts RBC
WBC
protein
hyaline
E. Complications of Acute Tubular Necrosis
Cardiovascular involvement
tissue edema
pulmonary edema
hypertension - due to fluid overload
congestive heart failure
arrythmias- due to acidosis & increased levels of serum potassium
Hyperkalemia (aka potassium intoxication) -increased potassium levels
tissue destruction in the kidneys (cellular breakdown)
acidosis(drives the potassium out of the cells into the blood)
kidneys don’t excrete potassium well
Severe hyperkalemia predisposition
cardiac arrythmias (bradycardia)
hemolysis of RBC’s
necrosis
Serum potassium levels greater than 5.5 - 6.0 mg / dl triggers the use of dialysis
Infection
the most common complication of ATN
Signs & symptoms often mimic ATN
Neurologic complaints - (nearly dead)
lethargy, coma, & grand malsiezures (convulsons)
usually attributed to hyponatremia (low serum sodium)
usually pt.s lose sodium w/ urine b/c of faulty aldosterone function
the systemic overload of fluid further complicates the hyponatremia by diluting the existing serum
Anemia
common in long standin ATN
secondary to the following:
decr. RBC production & decr. Erythropoetin from kidneys
incr. RBC destruction
acidosisis / azotemia causes RBC hemolysis
F. Special types of Acute Tubular Necrosis
Lack of oliguric phase
patients excrete excess sodium (an osmotic dieresis)
aldosteroe malfunction
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patients are “sodium wasters”
urinalysis shows incr. Sodium & decr. Potasium
amount of urine produced is fixed at 1000 ml/ per day
oblivious to outside measure
Tubular wall necrosis
Edema
Complications
hyponatremia
patients excrete more sodium even though they are sodium depleted initially
treatment goal is to restore sodium
dehydration
the tubules undergo a delayed response
the diuretic phase continues
treatment goal is to restore water
G. Recovery from ATN
the sign of recovery is "diuresis"
patients can die during this diuretic phase due to increased sodium & water loss
ATN has a higher mortality rate compared to AGN, especially with cortical nephron involvement
(50%)
cortical ATN leads to glomerular necrosis & eventual total renal shutdown
ATN in pregnancy has a poor prognosis
the main causative factor is electrolyte imbalance
azotemia reverses over a few weeks
anemia reverses over a few weeks (4-6) after recovery of kidney function
ATN usually leaves some residual kidney dysfunction
H. Diagnosis Credentials of ATN
oliguria
increased urine sodium concentration
urine constituents
Chronic Renal Failure (CRF)
A. Occurrence
gradual (from 6 months to 15 years)
the most common cause is diabetic neuropathy ( -> nephro calcinosis)
repeat insults - each episode damages more of the kidney until we start to lose some functional capacity
B. Progression
worsens over time
poor prognosis
progressive and generally irreversible decline in GFR
usually results in death
C. clinical Signs of CRF
anemia
osteodystrophy
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lipiduria
bilateral small kidney
neuropathy
increased serum uric acid levels
D. Characteristics of CRF
resembles acute renal failure except it takes longer to occur
some patients start with ARF & CRF
usually a diagnosis of length
amount of functioning nephrons are less than the critical amount needed for normal renal demands
the entire nephron is involved in the disease process
surviving nephrons look normal
E. Pathophysiology of CRF
decrease number of functioning nephrons -> decreased GFR -> increased BUN -> increased urinary sodium
F. Clinlcal Features of Chronic Renal Failure
Decreased GFR
Increased BUN due to decreased GFR
causes an increase in urea resorption
Hyponatremia
due to decreased reabsorption of sodium by the tubules surviving nephrons have an
increased blood flow so
there is less time for sodium absorption
sodium remains in the urine
Polyuria due to decreased sodium absorption in the tubules
the sodium draws the water out into the tubules
tends to involve the active transport mechanism for sodium
occurs in the early stages of CRF
patients have a history of waking at night to urinate
Dehydration due to polyuria
patients are hungry in the morning but usually don't eat due to the dehydration induced nausea
treatment goal is to increase fluid intake to combat the resultant dehydration of polyuria
Polydipsia - increased thirst
Factors
1. Increased BUN
2. Salt wasting
3. Excess urine (polyuria)
CRF develops at a slower rate if patient is well hydrated
Clinical Features of Chronic Renal Failure
Features Notes
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Oliguria occurs late in the disease process
when GFR approaches 10-20% of normal
treatment for this is to restrict fluid intake
these patients look similar to ARF patients
Diarrhea common symptom that contributes to sodium depletion
due to increased BUN
Nausea due to increased BUN
Early K+ problems patients excrete K+ so blood levels remain low
(polyuric state) tubular sodium influences aldosterone mechanism
incr. tubular sodium
incr. aldosterone release
incr. sodium resorption & K+ excretion
Late K+ problems factors behind hyperkalemia
(during oliguric state) poor potassium excretion (decr.d aldosterone effect)
Renal Tubular Acidosis common sign in CRF
factors of distal tubule dysfunction
failure to excrete excess acid
decreased bicarbonate ion resorption
Type I
distal tubule dysfunction
inability to excrete hydrogen
alkalotic urine (P.H. > 5.5)
Type II
proximal tubule dysfunction
bicarbonate ion resorption dysfunction
acidic urine ( 20 bacterial w/ hpf WBC's present (bacteruria)
greater than 5 WBC/ high power field = pyuria)
.
Tubules _> Glomeruli
F. Conditions Associated with Kidney Infection
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Obstruction
internal
stones, decr. peristalsis
external
prostate, tumor
Pregnancy
7% have bacteria in their urine
40% will develop pyelonephritis if untreated
theories for increased UTI incidence
dilation of uereters
fetal pressure on UG structures
Other Conditions
preexisting renal disease
diabetes mellitus
hypertension
decreased defense mechanisms (lowered immunity)
G. Urinary Tract Infection Treatment
acidify urine
antibiotics
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